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垂体肿瘤的发病机制。

Pathogenesis of pituitary tumors.

机构信息

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

出版信息

Prog Brain Res. 2010;182:207-27. doi: 10.1016/S0079-6123(10)82009-6.

Abstract

Pituitary tumors are common and mostly benign neoplasia which cause excess or deficiency of pituitary hormones and compressive damage to adjacent organs. Oncogene activation [e.g. PTTG (pituitary tumor-transforming gene) and HMGA2], tumor suppressor gene inactivation (e.g. MEN1 and PRKAR1A), epigenetic changes (e.g. methylation) and humoral factors (e.g. ectopic production of stimulating hormones) are all possible pituitary tumor initiators; the micro-environment of pituitary tumors including steroid milieu, angiogenesis and abnormal cell adhesion further promote tumor growth. Senescence, a cellular defence mechanism against malignant transformation, may explain the benign nature of at least some pituitary tumors. We suggest that future research on pituitary tumor pathogenesis should incorporate systems approaches, and address regulatory mechanisms for pituitary cell proliferation, development of new animal models of pituitary tumor and isolation of functional human pituitary tumor cell lines.

摘要

垂体肿瘤很常见,大多为良性肿瘤,可导致垂体激素过多或不足,并对邻近器官造成压迫性损伤。癌基因激活[如 PTTG(垂体肿瘤转化基因)和 HMGA2]、抑癌基因失活(如 MEN1 和 PRKAR1A)、表观遗传改变(如甲基化)和体液因素(如刺激激素的异位产生)都可能是垂体肿瘤的启动因素;垂体肿瘤的微环境包括类固醇环境、血管生成和异常细胞黏附,进一步促进肿瘤生长。衰老,一种针对恶性转化的细胞防御机制,可能解释了至少一些垂体肿瘤的良性性质。我们建议,未来对垂体肿瘤发病机制的研究应采用系统方法,并解决调节垂体细胞增殖的机制、建立新的垂体肿瘤动物模型以及分离功能性人垂体肿瘤细胞系。

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